Uphold our charter, says king: RESPECT LAWS: Ruler urges Malaysians not to undermine peace, harmony

YANG diPertuan Agong Sultan Abdul Halim Mu'adzam Shah yesterday said he is concerned with the attitude of some quarters in challenging the laws in the country,including the Federal Constitution. He said their actions could undermine the peace and harmony enjoyed by people in the country. Although Islam is the official religion of the federation, he said the Constitution also provides freedom for non-Muslims to practise their religious faiths."As head of the country, I wish to bring to attention the roles, responsibilities and obligations of all quarters to safeguard the country's peace and harmony."The people should always respect and uphold the law," he said when opening Universiti Utara Malaysia's (UUM) 26th convocation here yesterday

A Guyon's canal ganglion presenting as occupational overuse syndrome: A case report

<p>Abstract</p> <p>Background</p> <p>Occupational overuse syndrome (OOS) can present as Guyon's canal syndrome in computer keyboard users. We report a case of Guyon's canal syndrome caused by a ganglion in a computer user that was misdiagnosed as OOS.</p> <p>Case presentation</p> <p>A 54-year-old female secretary was referred with a six-month history of right little finger weakness and difficulty with adduction. Prior to her referral, she was diagnosed by her general practitioner and physiotherapist with a right ulnar nerve neuropraxia at the level of the Guyon's canal. This was thought to be secondary to computer keyboard use and direct pressure exerted on a wrist support. There was obvious atrophy of the hypothenar eminence and the first dorsal interosseous muscle. Both Froment's and Wartenberg's signs were positive. A nerve conduction study revealed that both the abductor digiti minimi and the first dorsal interosseus muscles showed prolonged motor latency. Ulnar conduction across the right elbow was normal. Ulnar sensory amplitude across the right wrist to the fifth digit was reduced while the dorsal cutaneous nerve response was normal. Magnetic resonance imaging of the right wrist showed a ganglion in Guyon's canal. Decompression of the Guyon's canal was performed and histological examination confirmed a ganglion. The patient's symptoms and signs resolved completely at four-month follow-up.</p> <p>Conclusion</p> <p>Clinical history, occupational history and examination alone could potentially lead to misdiagnosis of OOS when a computer user presents with these symptoms and we recommend that nerve conduction or imaging studies be performed.</p

Cauli: a mouse strain with an Ift140 mutation that results in a skeletal ciliopathy modelling jeune syndrome

Cilia are architecturally complex organelles that protrude from the cell membrane and have signalling, sensory and motility functions that are central to normal tissue development and homeostasis. There are two broad categories of cilia; motile and non-motile, or primary, cilia. The central role of primary cilia in health and disease has become prominent in the past decade with the recognition of a number of human syndromes that result from defects in the formation or function of primary cilia. This rapidly growing class of conditions, now known as ciliopathies, impact the development of a diverse range of tissues including the neural axis, craniofacial structures, skeleton, kidneys, eyes and lungs. The broad impact of cilia dysfunction on development reflects the pivotal position of the primary cilia within a signalling nexus involving a growing number of growth factor systems including Hedgehog, Pdgf, Fgf, Hippo, Notch and both canonical Wnt and planar cell polarity. We have identified a novel ENU mutant allele of Ift140, which causes a mid-gestation embryonic lethal phenotype in homozygous mutant mice. Mutant embryos exhibit a range of phenotypes including exencephaly and spina bifida, craniofacial dysmorphism, digit anomalies, cardiac anomalies and somite patterning defects. A number of these phenotypes can be attributed to alterations in Hedgehog signalling, although additional signalling systems are also likely to be involved. We also report the identification of a homozygous recessive mutation in IFT140 in a Jeune syndrome patient. This ENU-induced Jeune syndrome model will be useful in delineating the origins of dysmorphology in human ciliopathies

Fenazin sebagai potensi antibiotik baru daripada Streptomyces kebangsaanensis

Fenazin merupakan metabolit sekunder yang biasanya disintesis secara semula jadi oleh Pseudomonas dan Streptomyces. Ia merupakan sebatian heterosiklik yang mempunyai sebatian bernitrogen pada struktur teras cecincin. Kajian mengenai antibiotik ini telah bermula seawal abad ke-19 lagi dan ternyata menjadi calon dadah yang berpotensi tinggi dalam dunia perubatan. Sehingga kini, lebih daripada 100 jenis fenazin telah diterokai daripada sumber semula jadi dan boleh bertindak sebagai antibakteria, antikanser, antivirus, antitumor serta antiparasit. Setakat ini, kajian biosintesis fenazin yang telah dijalankan terhadap Pseudomonas dan Streptomyces telah mendedahkan gen yang bertanggungjawab dalam tapak jalan biosintesis fenazin, namun begitu, gen khusus yang terlibat dalam penghasilan terbitan fenazin yang kompleks masih dalam hipotesis. Dalam ulasan ini, kami membincangkan kepentingan fenazin serta pemahaman terkini tentang tapak jalan biosintesis fenazin yang berjaya diterokai di dalam Streptomyces kebangsaanensis

Supporting field study with personalized project spaces in a geographical digital library

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Cerebral hypomyelination associated with biallelic variants of FIG4

The lipid phosphatase gene FIG4 is responsible for Yunisâ Varón syndrome and Charcotâ Marieâ Tooth disease Type 4J, a peripheral neuropathy. We now describe four families with FIG4 variants and prominent abnormalities of central nervous system (CNS) white matter (leukoencephalopathy), with onset in early childhood, ranging from severe hypomyelination to mild undermyelination, in addition to peripheral neuropathy. Affected individuals inherited biallelic FIG4 variants from heterozygous parents. Cultured fibroblasts exhibit enlarged vacuoles characteristic of FIG4 dysfunction. Two unrelated families segregate the same Gâ >â A variant in the +1 position of intron 21 in the homozygous state in one family and compound heterozygous in the other. This mutation in the splice donor site of exon 21 results in readâ through from exon 20 into intron 20 and truncation of the final 115 Câ terminal amino acids of FIG4, with retention of partial function. The observed CNS white matter disorder in these families is consistent with the myelination defects in the FIG4 null mouse and the known role of FIG4 in oligodendrocyte maturation. The families described here the expanded clinical spectrum of FIG4 deficiency to include leukoencephalopathy.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/1/humu23720-sup-0001-Supp_Mat_Lenk_2018.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/2/humu23720.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/3/humu23720_am.pd